Original Article

Molecular Psychiatry (2016) 21, 261–269; doi:10.1038/mp.2015.29; published online 31 March 2015

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

M Hornig1,2, G Gottschalk3, D L Peterson3, K K Knox4,5, A F Schultz1, M L Eddy1, X Che1 and W I Lipkin1,2,6

  1. 1Center for Infection and Immunity, Columbia University Mailman School of Public Health, New York, NY, USA
  2. 2Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA
  3. 3Sierra Internal Medicine at Incline Village, Incline Village, NV, USA
  4. 4Coppe Healthcare Solutions, Waukesha, WI, USA
  5. 5Simmaron Research, Incline Village, NV, USA
  6. 6Departments of Pathology and Neurology, College of Physicians and Surgeons, Columbia University, New York, NY, USA

Correspondence: Dr M Hornig, Center for Infection and Immunity, Columbia University Mailman School of Public Health, 722 West 168th Street, Room 1706, New York, NY 10032, USA. E-mail: mh2092@cumc.columbia.edu

Received 20 November 2014; Revised 19 January 2015; Accepted 9 February 2015
Advance online publication 31 March 2015

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Abstract

Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.